Evidence map›Paper›PMID 36670319›Full record

ReviewCurrent treatment options in oncology2023

Autophagy Paradox: Strategizing Treatment Modality in Melanoma.

Christian Pangilinan, Xiaowei Xu, Meenhard Herlyn, Chengyu Liang

Abstract readReview
In one paragraph

Review in Current treatment options in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Article
  2. Terpenoids as modulators of autophagy-senescence crosstalk in lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  3. Autophagy in Melanoma: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Mitochondrial bioenergetics and networks in melanoma: an update.Apoptosis : an international journal on programmed cell death · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Christian PangilinanMolecular and Cellular Oncogenesis Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA, 19104, USA.ORCID 0000-0003-3913-7912
Xiaowei XuDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Meenhard HerlynMolecular and Cellular Oncogenesis Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA, 19104, USA.
Chengyu LiangMolecular and Cellular Oncogenesis Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA, 19104, USA. cliang@wistar.org.ORCID 0000-0001-6082-2143

Funding

Role of UVRAG-mediated Autophagy in Tumor SuppressionR01CA140964 · NCI · WISTAR INSTITUTE · PI LIANG, CHENGYU · 2009 to 2025
$5.4M
Molecular Mechanism of UV Protection in Cutaneous MelanomaR01ES029092 · NIEHS · WISTAR INSTITUTE · PI LIANG, CHENGYU · 2019 to 2023
$3.0M
A cancer-derived truncating mutation in disease penetrance and progression of MSI CRCR01CA238457 · NCI · WISTAR INSTITUTE · PI LIANG, CHENGYU · 2020 to 2024
$2.9M
New control of oncogene activation in T-cell leukemiaR01CA262631 · NCI · WISTAR INSTITUTE · PI Chengyu Liang · 2022 to 2026
$2.6M
NCI NIH HHS R01 CA140964NCI NIH HHS R01 CA238457NCI NIH HHS R01 CA262631NIEHS NIH HHS R01 ES029092
6 · The paper itself

Abstract

opinion statementThe primordial autophagy process, originally identified as a starvation response in baker's yeast, has since been shown to have a wide spectrum of functions other than survival. In many cases, it is accepted that autophagy operates as a key tumor suppressor mechanism that protects cells from adverse environmental cues by enforcing homeostasis and maintaining the functional and structural integrity of organelles. Paradoxically, heightened states of autophagy are also seen in some cancers, leading to the prevailing view that the pro-survival aspect of autophagy might be hijacked by some tumors to promote their fitness and pathogenesis. Notably, recent studies have revealed a broad range of cell-autonomous autophagy in reshaping tumor microenvironment and maintaining lineage integrity and immune homeostasis, calling for a renewed understanding of autophagy beyond its classical roles in cell survival. Here, we evaluate the increasing body of literature that argues the "double-edged" consequences of autophagy manipulation in cancer therapy, with a particular focus on highly plastic and mutagenic melanoma. We also discuss the caveats that must be considered when evaluating whether autophagy blockade is the effector mechanism of some anti-cancer therapy particularly associated with lysosomotropic agents. If autophagy proteins are to be properly exploited as targets for anticancer drugs, their diverse and complex roles should also be considered.

Indexed as

Antineoplastic AgentsMelanomaNeoplasmsAutophagyCell SurvivalHumansTumor MicroenvironmentAntineoplastic AgentsAutophagyImmunotherapyLysosomeMelanomaSkin cancerTargeted therapy

Identifiers

PMID36670319
PMCPMC9883356

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.